An Acute Experimental Model Demonstrating 2 Different Forms of Sustained Atrial Tachyarrhythmias

Abstract

Background-The objective of this study was to develop an acute experimental model showing both focal and macroreentrant sustained atrial fibrillation (AF). Methods and Results-In 31 anesthetized dogs, bilateral thoracotomies allowed the attachment of electrode catheters at the right and left superior pulmonary veins, atrial free walls, and atrial appendages. Acetylcholine, 100 mmol/L, was applied topically to either appendage. Sequential radiofrequency ablation was achieved for the ganglionated plexi (GP), found adjacent to the 4 pulmonary veins. In 12 separate studies, a propafenone bolus, 2 mg/kg, was given before and after GP ablations at the start of acetylcholine-induced AF. Acetylcholine caused abrupt onset of AF (nϭ22) or induced AF by burst pacing (nϭ9) that lasted Ն10 minutes. Rapid, regular, or fractionated atrial electrograms were consistently seen (average cycle length, 37Ϯ7 ms) at the appendages versus cycle lengths of 114Ϯ23 ms at other atrial sites. After ablations of GP, AF abruptly terminated (nϭ25). In 6 dogs, sustained atrial tachyarrhythmias continued. Pacing at specific atrial sites organized electrograms of one atrium or also captured the other atrium. The latter resulted in termination when pacing was stopped in 4 of these 6 experiments. Propafenone did not change the duration of focal AF before GP ablation (17Ϯ9 versus 14Ϯ8 minutes; control, Pϭ0.6) but terminated reentrant atrial tachyarrhythmias (12Ϯ3 versus 2Ϯ1 minutes, Pϭ0.0009). Conclusions-Before GP ablation, acetylcholine (100 mmol/L) induced sustained AF characterized by rapid, focal firing.GP ablations were associated with loss of focal firing and regularization of electrograms in both atria before termination. Propafenone failed to terminate focal AF but rapidly terminated entrainable macroreentrant atrial tachyarrhythmias. (Circ Arrhythmia Electrophysiol. 2009;2:384-392.)

Nature of Electrogram Fractionation During Atrial Fibrillation

“…Sequential ablation of 4 fat pads, each containing a GP (located far from the appendage), without injuring the atrial myocardium, produced progressive slowing and organization of electrograms in the atria (and in the appendage), followed by the elimination of firing in the appendage and termination of AF. 22 This response is similar to the progressive slowing and electrogram organization observed during the stepwise ablation for persistent AF, previously introduced by the authors of the present study. 23 The fractionated electrogram ablation sites most frequently associated with termination of AF are located in the same regions as the GP, supporting the possible role of inadvertent GP ablation in electrogram organization in these patients.…”

Use of endogenous NADH fluorescence for real-time in situ visualization of epicardial radiofrequency ablation lesions and gaps

“…If implemented clinically, it has the potential to shorten the time and improve the efficiency of ablations, minimize unnecessary tissue injury that may cause post-RFA complications, and decrease postablation recurrence of arrhythmias. fNADH imaging may also be useful for mechanistic studies of tissue injury near the RFA sites (28) and for assessment of drugs that may alter electrical propagation between interlesion gaps (27). We also believe that NADH fluorescence could be potentially very useful in identifying the ablation gaps seen after pulmonary vein isolation procedures.…”

Left Atrial Wall Stress Distribution and Its Relationship to Electrophysiologic Remodeling in Persistent Atrial Fibrillation

“…This is in keeping with other recent studies showing that CFAE are not associated with areas of low voltage 36,37,39 -41 but is at odds with conventional wisdom. 30 Focal remodeling might be expected to contribute to zones of slow conduction, pivot points or block, 42 and resultant micro-or macro-reentry 43 but is less likely to bear any relationship to rotors or rapidly discharging foci that may be more dependent on autonomic drive and proximity to ganglionated plexi. 43 Therefore, although atrial remodeling promotes AF, 2-10 peaks in wall stress and areas of remodeling are actually less likely to support CFAE.…”